Figure 145

The tubuloglomerular (TG) feedback mechanism. A, Normal TG feedback. In the normal kidney, the TG feedback mechanism is a sensitive device for the regulation of the single nephronglomerular filtration rate (SNGFR). Step 1: An increase in SNGFR increases the amount of sodium chloride (NaCl) delivered to the juxtaglomerular apparatus (JGA) of the nephron. Step 2: The resultant change in the composition of the filtrate is sensed by the macula densa cells and initiates activation of the JGA. Step 3: The JGA releases renin, which results in the local and systemic generation of angiotensin II. Step 4: Angiotensin II induces vasocontriction of the glomerular arterioles and contraction of the mesangial cells. These events return SNGFR back toward basal levels. B, TG feedback in ARF. Step 1: Ischemic or toxic injury to renal tubules leads to impaired reabsorption of NaCl by injured tubular segments proximal to the JGA. Step 2: The composition of the filtrate passing the macula densa is altered and activates the JGA. Step 3: Angiotensin II is released locally. Step 4: SNGFR is reduced below normal levels. It is likely that vasoconstrictors other than angiotensin II, as well as vasodilator hormones (such as PGI2 and nitric oxide) are also involved in modulating TG feedback. Abnormalities in these vasoactive hormones in ARF may contribute to alterations in TG feedback in ARF.